Bremia lactucae, an oomycete, is the causal organism of downy mildew in lettuce (Lactuca sativa L.), and constitutes a major problem for lettuce production in both glass house and open field conditions. Bremia lactucae is an obligate parasite capable of infecting a lettuce plant in any growth stage from seedling to mature plant.
Downy mildew causes pale, angular, yellow areas bounded by veins on the upper leaf surfaces. Spore formation appears on the lower leaf surface as a white cottony-like fungal growth soon after initial symptom development. The lesions eventually turn brown, and they may enlarge and coalesce. These symptoms typically occur first on the lower leaves of the lettuce, but under ideal conditions may move into the upper leaves of the head. When the oomycete progresses to this degree, the head cannot be harvested. Less severe damage requires the removal of more leaves than usual, especially when the lettuce reaches its final destination. As such, every year this disease leads to millions of dollars of lost lettuce crop throughout the world.
Breeding for lettuce resistant against Bremia lactucae has been based upon the identification and introgression of resistance genes (R-genes), known in lettuce as Dm genes. When R-gene products of a lettuce plant recognize specific Bremia avirulence (Avr) gene products in a gene-for-gene interaction, this triggers downstream response pathways in the host plant. The result is an incompatible reaction associated with a hypersensitive cell death response by the host plant, thus providing race-specific resistance against Bremia lactucae. 
However, R-genes may be rendered ineffective soon after they are introduced due to the rapid genetic adaption of the pathogen. As new Bremia lactucae races or isolates emerge, their Avr genes have been altered in such a way that allows the pathogen to evade recognition by the host and overcome race-specific resistance. Recognition of the altered Avr genes by existing R-genes is thus lost, and infection by newly emergent Bremia lactucae races or isolates can successfully be established resulting in disease. Re-establishment of resistance in the plant can only occur however, if novel R-genes are introduced into the plant which are able to recognize other Avr genes. Thus, the continual co-evolution of the plant and the pathogen has led to a so-called arms race.
The aforementioned arms race between the plant and the pathogen is a continuous evolutionary struggle. For the lettuce plant, this means that the resistance provided by existing R-genes are broken. Thus breeders require novel resistance genes in order to keep producing resistant varieties.
One breeding technique used to slow down the rapid adaption by newly emerging Bremia races or isolates is to stack or pyramid different R-genes, in order to provide new combinations of R-genes. R-genes are grouped together in a limited number of locations on the lettuce genome, known as resistance clusters. In lettuce, major resistance clusters are known to be located on linkage group 1, linkage group 2, linkage group 4, and linkage group 8 (linkage groups are numbered according to the integrated genetic map of lettuce, Truco et. al. (2007) Theoretical and Applied Genetics, 115(6): 735-46). R-genes from the same cluster can segregate as alleles or tightly linked genes. Therefore, it is often impossible to stack R-genes from the same cluster because genes on the same cluster are in repulsion phase (e.g. allelic) with one another and inherit like alternative alleles of the same locus. By combining R-genes and alleles from different clusters, in coupling phase, more durable forms of resistance may be bred. Moreover, novel R-genes with the potential to be stacked with existing R-genes are an extremely valuable asset to the breeder since the breeder has new stacking possibilities at hand, thus slowing down the virulence of the pathogen.
Quantitative Trait Loci (QTLs) for Bremia resistance derived from L. saligna CGN5271 have also been described, such as rbq1, rbq2 and rbq3, located on chromosome 7, 1 and 9 respectively (Jeuken et al. 2008, Theor Appl Genet 116: 845-857 and Jeuken and Lindhout 2002, Theor Appl Genet 105: 384-391). The recessive QTL rbq3 is located on the upper half of chromosome 9.
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